Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1995-2-23
pubmed:abstractText
The objective of this investigation was to determine the effect of cultured human umbilical vein endothelial cells (HUVEC) on the vascular response to canine coronary arteries in which the endothelium had been either mechanically removed or injured by multiple brief episodes of occlusion and reperfusion in vivo. The endothelium-dependent vasodilator, A23187 (10(-6) mol/l) did not cause any significant relaxation in vessels from which the endothelium had been removed. However, following addition of cultured HUVEC to the tissue bath (75 x 10(3) cells/ml), A23187 produced a significant (p < 0.05) relaxation. This effect was abolished by inhibition of nitric oxide synthase with Nw-nitro-l-arginine methyl ester (L-NAME). Vascular relaxation caused by the nitric oxide donor SIN-1 was significantly (p < 0.05) enhanced when cultured HUVEC were added to vessels mechanically denuded of endothelium. Repetitive ischemia and reperfusion significantly inhibited the relaxant response to A23187. Addition of cultured HUVEC to the tissue bath partially restored the response to A23187. In contrast to the mechanically damaged vessels the relaxant response to SIN-1 was unaffected by cultured HUVEC in reperfusion-injured vessels. These results demonstrate that cultured endothelial cells partially restore endothelium-dependent vasodilation of vessels in which the endothelium is not functional following mechanical- or reperfusion-induced damage. The differential effect of endothelial cells on the response to SIN-1 suggests that mechanical and reperfusion injury alter the coronary vascular response to SIN-1 by different mechanisms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0031-7012
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
249-56
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7831388-Animals, pubmed-meshheading:7831388-Arginine, pubmed-meshheading:7831388-Blood Flow Velocity, pubmed-meshheading:7831388-Calcimycin, pubmed-meshheading:7831388-Cells, Cultured, pubmed-meshheading:7831388-Coronary Circulation, pubmed-meshheading:7831388-Coronary Disease, pubmed-meshheading:7831388-Coronary Vessels, pubmed-meshheading:7831388-Dogs, pubmed-meshheading:7831388-Dose-Response Relationship, Drug, pubmed-meshheading:7831388-Endothelium, Vascular, pubmed-meshheading:7831388-Molsidomine, pubmed-meshheading:7831388-Muscle, Smooth, Vascular, pubmed-meshheading:7831388-Muscle Relaxation, pubmed-meshheading:7831388-Myocardial Contraction, pubmed-meshheading:7831388-Myocardial Reperfusion Injury, pubmed-meshheading:7831388-NG-Nitroarginine Methyl Ester, pubmed-meshheading:7831388-Nitric Oxide, pubmed-meshheading:7831388-Umbilical Veins, pubmed-meshheading:7831388-Vasodilator Agents
pubmed:year
1994
pubmed:articleTitle
Cultured endothelial cells restore vasodilator responses to coronary arteries with impaired endothelial function and alter the response to a nitric oxide donor.
pubmed:affiliation
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.